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Tissue mitochondrial activity dictates the macrophage pool size.

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dc.contributor.authorPena-Couso, Laura
dc.contributor.authorSicilia, Jon
dc.contributor.authorVieto, Sofía
dc.contributor.authorSilva-Rojas, Roberto
dc.contributor.authorSánchez-Díaz, María
dc.contributor.authorCalvo, Enrique
dc.contributor.authorRomero-Becerra, Rafael
dc.contributor.authorFolgueira, Cintia
dc.contributor.authorHerrera-Melle, Leticia
dc.contributor.authorJusto-Méndez, Raquel
dc.contributor.authorHong, Xiaotong
dc.contributor.authorCampanario, Silvia
dc.contributor.authorLópez, Juan A
dc.contributor.authorCrainiciuc, Georgiana
dc.contributor.authorGil, María
dc.contributor.authorMartín-Salamanca, Sandra
dc.contributor.authorLukesova, Vera
dc.contributor.authorSegalés, Jessica
dc.contributor.authorSerrano, Antonio L
dc.contributor.authorBallesteros, Iván
dc.contributor.authorLeón, Marta
dc.contributor.authorde Andrés-Laguillo, Macarena
dc.contributor.authorStifter, Sebastian A
dc.contributor.authorEsteban-Martínez, Lorena
dc.contributor.authorIsern, Joan
dc.contributor.authorAlegre-Cebollada, Jorge
dc.contributor.authorTorres, Miguel
dc.contributor.authorGreter, Melanie
dc.contributor.authorVázquez, Jesús
dc.contributor.authorEnríquez, José A
dc.contributor.authorSabio-Buzo, Guadalupe
dc.contributor.authorMuñoz-Cánoves, Pura
dc.contributor.authorHidalgo, Andrés
dc.contributor.authorNicolás-Ávila, José A
dc.date.accessioned2026-09-15T09:50:42Z
dc.date.available2026-09-15T09:50:42Z
dc.date.issued2026-09-04
dc.description.abstractRemoval of cellular waste from the extracellular space is fundamental for tissue health. Because the rate of material ejected by parenchymal cells varies across tissues, we searched for mechanisms that couple waste production and removal. Here, we show that the uptake of parenchyma-released mitochondria by macrophages is prominent across organs that rely on oxidative respiration-including heart, skeletal muscle, and brown adipose tissue-and that macrophage numbers closely align with the mitochondrial activity of each of these organs. We found that the mitochondrial activity of myofibers dictates the abundance of macrophages by modulating colony-stimulating factor 1 (CSF1) availability and the number of CSF1-producing fibroblasts in the tissue. Consequently, inhibition of CSF1-CSF1 receptor (CSF1R) signaling depleted macrophages and collapsed the mitochondrial activity of skeletal muscles. We propose that, by coupling macrophage abundance to the mitochondrial activity of their parenchyma, tissues ensure efficient waste disposal and fitness.
dc.description.peerreviewedSí
dc.description.tableofcontentsA.H. was supported by HR17_00527 from Fundacion La Caixa, the Transatlantic Network of Excellence (TNE-18CVD04) from the Leducq Foundation, and FET-OPEN (no. 861878) from the European Commission. P.M.- C. was supported by MICIU-Spain (RTI2018-096068), ERC-2016-AdG-741966, and the Maria de Maeztu Program for Units of Excellence to UPF (MDM-2014-0370). J.A.N.-A. was supported by the University of California San Francisco (UCSF) Cardiovascular Research Institute (CVRI) department, the UCSF Dean's office program, the Pilot Feasibility Award from the UCSF-NORC (funded by NIH: P30DK098722 grant), and the Sandler Program for Breakthrough Biomedical Research (PBBR), which is partially funded by the Sandler Foundation. G.S. was supported by PID2022-138525OB-I00 funded by MICIU/AEI/10.13039/501100011033 NextGenerationEU/PRTR, and G.S. and J.V. were funded by IMPACT-2021 PMP21/00113 Instituto de Salud Carlos III. J.A.E. was supported by ERC-2024-AdG (101198761) and PID2024-158440OB-I00, PID2021-1279880B-100, and TED2024-158440OB-I00 funded by MCIU/AEI/10.13039/501100011033 and the European Union "NextGenerationEU"/Plan de Recuperacion Transformacion y Resiliencia/PRTR and by CIBERFES (CB16/10/00282). M. Greter was supported by the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (grant agreement no.819229).J.A.-C. acknowledges funding from the Ministerio de Ciencia, Innovacion y Universidades (MICIU, MICIU/AEI/10.13039/501100011033) through grant PID2023-147683NB-I00 [European Regional Development Fund (ERDF)]. M.T. was supported by Comunidad de Madrid grant P2022/BMD-7245 and ERC-AdG REACTIVA Ref. 101142005. S.V. was supported by the AHA Predoctoral Fellowship, grant no. 24PRE1181771. C.F. was funded by a Sara Borrell fellowship (CD19/00078), the NNF23SA0083952-EASO/Novo Nordisk New Investigator Award in Basic Sciences 2023, the EFSD/Lilly Young Investigator Award 2022, the Society for Endocrinology/Early Career Grant 2022, and FSEEN/Jovenes endocrinologos 2022. I.B. was supported by grants from MICIN (RYC2020-029563-I and PID2022-140534NB-I00). L.E.-M. was supported by Juan de la Cierva Incorporacion (IJC2020-045688-I) from Ministerio de Ciencia e Innovacion (MCIN). R.J.-M. was supported by MICIU fellowship (PRE2019-087462). J.V. acknowledges grants PID2021-122348NB-I00 and PID2024-155650NB-I00 funded by MICIU and by "ERDF A way of making Europe"; PLEC2022-009298, PLEC2022-009235, and EQC2021-007053-P funded by MICIU and by "European Union NextGenerationEU/PRTR"; S2022/BMD-7333-CM (INMUNOVAR-CM) funded by Comunidad de Madrid; and LCF/PR/HR22/52420019 funded by "la Caixa" Foundation. The CNIC is supported by the MCIN, the Instituto de Salud Carlos III, and the Pro-CNIC Foundation and is a Severo Ochoa Center of Excellence (grant number CEX2020-001041-S funded by MCIU/AEI/10.13039/501100011033).
dc.format.number123
dc.format.volume11
dc.identifier.citationSci Immunol. 2026 Sep 4;11(123):eaeb9244.
dc.identifier.journalSCIENCE IMMUNOLOGY
dc.identifier.pubmedID42696609
dc.identifier.urihttps://hdl.handle.net/20.500.12105/27714
dc.language.isoeng
dc.publisherAMER ASSOC ADVANCEMENT SCIENCE
dc.relation.isreferencedbyPubMed
dc.relation.publisherversion10.1126/sciimmunol.aeb9244
dc.repisalud.institucionCNIC
dc.rights.accessRightsmetadata only access
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleTissue mitochondrial activity dictates the macrophage pool size.
dc.typeresearch article
dc.type.hasVersionNA
dspace.entity.typePublication

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